ライフサイエンスコーパス: focal contact

1 ) that are aligned in parallel converging at focal contacts.

2 gh the chimeric molecule was targeted to the focal contacts.

3 ibronectin fibrillogenesis without affecting focal contacts.

4 function of the Pak1-betaPIX-GIT complex at focal contacts.

5 l-extracellular matrix associations known as focal contacts.

6 Cell-cell adhesions were more sensitive than focal contacts.

7 in-like cytoskeleton staining extending into focal contacts.

8 ronectin-induced localization of paxillin to focal contacts.

9 did not inhibit alpha5beta1 localization to focal contacts.

10 Paxillin LIM domains mediate localization to focal contacts.

11 bserved as linear streaks and beta3 found in focal contacts.

12 orylation and of tyrosine phosphorylation of focal contacts.

13 ocked class I-induced paxillin assembly into focal contacts.

14 cupied integrin receptors do not localize to focal contacts.

15 ess fiber formation and decreased numbers of focal contacts.

16 tion upon ligand binding and is localized in focal contacts.

17 which affects cell adhesion and formation of focal contacts.

18 integrin signaling compartments, designated focal contacts.

19 on the cell surface and did not localize to focal contacts.

20 tress-stimulated FAK Tyr-397 localization to focal contacts.

21 ting focal adhesion kinase redistribution to focal contacts.

22 diated localization of phosphorylated FAK to focal contacts.

23 ogue of RP748, localized to alpha(v)beta3 at focal contacts.

24 7 interaction with FAK or recruitment to the focal contacts.

25 c elicited a loss of actin stress fibers and focal contacts.

26 an-4, and it co-localizes with syndecan-4 in focal contacts.

27 m in a punctate fashion and is excluded from focal contacts.

28 K, which is required for FAK localization at focal contacts.

29 th many of the alphavbeta3 integrin-positive focal contacts.

30 grin-containing protein complexes outside of focal contacts.

31 association with F-actin and localization to focal contacts.

32 determine the impact of Pyk2 localization to focal contacts.

33 e of zyxin caused the loss of Mena/VASP from focal contacts.

34 ns interact with the cytoskeleton outside of focal contacts; 2) activation of a cell and activation o

35 in the cell center and excluded from nascent focal contacts along the circular lamellipodium, as reve

36 ctin-based adherens junction and cell/matrix focal contact anchoring junction type restricted to the

37 oes not inhibit cell adhesion, spreading, or focal contact and stress fiber formation.

38 es are lost, TLR signaling induces prominent focal contacts and a transient reduction in DC migratory

39 occupied alpha(5)beta(1) integrins away from focal contacts and along bundles of actin filaments gene

40 ed) has major effects on the organization of focal contacts and cytoskeleton and on directed cell mot

41 d in NIH 3T3 cells, DFak56 both localizes to focal contacts and displays the characteristic elevation

42 tegrins, leading to the formation of initial focal contacts and endothelial cell migration.

43 Y783,795F cells developed numerous fine focal contacts and exhibited motility on a surface.

44 ar matrix promotes the recruitment of FAK to focal contacts and increases in its phosphotyrosine cont

45 main eliminated partial Grb7 localization to focal contacts and its ability to stimulate cell migrati

46 -1034) inhibited Pyk2/FAK-CT localization to focal contacts and its capacity to promote cell motility

47 lts demonstrate a role for Grb7 targeting to focal contacts and its phosphorylation by FAK in the reg

48 nt of tyrosine phosphorylation events at the focal contacts and may therefore represent a novel pathw

49 ession dramatically reduced the formation of focal contacts and stress fibers in VSMCs by blocking th

50 integrins are mobile within the confines of focal contacts and that this mobility is supported by an

51 By usurping components from focal contacts and the actin cytoskeleton, the intracell

52 ce studies indicated that SHIP2 localized to focal contacts and to lamellipodia.

53 diated localization of phosphorylated FAK to focal contacts and treatment with the Rho-associated kin

54 s in the distribution of vinculin containing focal contacts, and altered temporal response of Cx43alp

55 e extensive actin cytoskeletal organization, focal contacts, and directionally persistent cell motili

56 spreading, formation of prominent peripheral focal contacts, and integrin-mediated activation of foca

57 ne for retaining ability to adhere, assemble focal contacts, and migrate is Y783.

58 However, cells were able to establish focal contacts, and single cell migration toward HGF was

59 s concentrated near the advancing edge where focal contacts are being formed and focal adhesion prote

60 lecules typically found in integrin-mediated focal contacts are not associated with TF.

61 ta3 integrin/2A3 antibody positively stained focal contacts are recognized by vinculin antibodies as

62 In actinin-4-knockdown keratinocytes, focal contact area is increased by 25%, and hemidesmosom

63 There was a significant increase in focal contact area when the force was removed (p < 0.01)

64 out the cytoplasm, while FAK is localized in focal contacts as expected, suggesting that the differen

65 llular fibronectin fibrils, and formation of focal contacts as indicated by punctate vinculin stainin

66 rins are not immobile when incorporated into focal contacts, as some have suggested.

67 ust alphavbeta6 integrin-induced, peripheral focal contacts associated with elaborate stress fibers.

68 or-like translocation occurs relative to the focal contacts at 6.5 +/- 0.7 microm/h and is independen

69 and thickening of F-actin microfilaments in focal contacts at the basolateral monolayer surface comp

70 bly plays a key role in the stabilization of focal contacts at the leading edge of migrating cells, t

71 These links occur not only at focal contacts but also at smaller integrin-containing p

72 lls, including assembly of stress fibers and focal contacts, but it did not induce reorganization of

73 fascin microspikes and increased assembly of focal contacts by cells adherent on thrombospondin-1.

74 red beta3 integrin and actinin-1 dynamics in focal contacts by using fluorescence recovery after phot

75 The focal contacts changed in position and contact area when

76 llenged HOK-16 cells revealed proteolysis of focal contact components (e.g., focal adhesion kinase),

77 ensin, but contain low levels of the typical focal contact components paxillin, vinculin, and tyrosin

78 These changes in focal contact composition were not due to a change in st

79 highly tyrosine-phosphorylated, "classical" focal contacts containing high levels of paxillin and vi

80 There was no significant change in focal contact coverage area before and after force appli

81 he Raf/MAPK pathway, led to stress fiber and focal contact disruption, whereas the adherens junctions

82 eins localize with alpha(v)beta3 integrin in focal contacts distributed towards the periphery of tran

83 v-Src-RT exhibited a partial perinuclear and focal contact distribution in Src-/- cells.

84 zation of plasminogen activators at sites of focal contact does not initiate a proteolytic cascade le

85 -cell and cell-matrix contact, distinct from focal contacts, even in the absence of serum.

86 e mutant by competing with endogenous FAK in focal contacts for binding signaling molecules such as S

87 stream MAP kinase activation, and associated focal contact formation and cell spreading.

88 moted apoptosis in HEK293 cells and impaired focal contact formation in podocytes.

89 ll spreading, cell-fibronectin adhesion, and focal contact formation in response to platelet-derived

90 s, and suggest a feedback mechanism by which focal contact formation might be initiated.

91 In addition, focal contact formation was enhanced as indicated by pax

92 ted with focal adhesion kinase and modulated focal contact formation, and exhibited frequent robust o

93 vbeta8 also induced cell rounding, inhibited focal contact formation, and initiated an inhibitory sig

94 nus of fibronectin modulates actin assembly, focal contact formation, tyrosine kinase activity, and c

95 sphorylation and subsequent stress fiber and focal contact formation.

96 mentin and RACK1 decreased cell adhesion and focal contact formation.

97 tion was dispensible for cell attachment and focal contact formation.

98 ere characterized by release of the cellular focal contacts from the glass substratum, followed by co

99 or tumorigenic growth, in part by regulating focal contacts in a PKC-dependent mechanism.

100 The protein is localized at focal contacts in adherent erythroleukemia cells.

101 ase in recruitment of alpha V integrins into focal contacts in alpha 5-null cells plated on FN, indic

102 mosomes, while alpha3beta1 is recruited into focal contacts in cultured cells.

103 mino acid protein, kindlin-1, a component of focal contacts in keratinocytes.

104 herent to vitronectin, paxillin localizes to focal contacts in the absence of FAK expression and is p

105 tegrin-dependent localization of paxillin to focal contacts in the absence of FAK expression.

106 ta3-integrin, which are at the core of these focal contacts, in cultured endothelial cells.

107 d forms adhesions structurally distinct from focal contacts, independent of actomyosin-mediated cell

108 we used single particle tracking to examine focal contact-independent cytoskeletal associations of a

109 We previously demonstrated the importance of focal contact-independent integrin-cytoskeleton interact

110 of beta1-integrins with the cytoskeleton at focal contacts interferes with integrin-mediated bacteri

111 n receptor alpha(5)beta(1) translocates from focal contacts into and along extracellular matrix (ECM)

112 The formation and remodeling of focal contacts is a dynamic process under the regulation

113 nt recruitment of a subset of c-Abl to early focal contacts is observed coincident with the export of

114 ) against the alpha4 laminin G domain stains focal contact-like structures in transformed and primary

115 llin, with their regulation by integrins and focal contact localization.

116 ne of these mutants, leading to constitutive focal contact localization.

117 l internalization, yet severely defective in focal contact localization.

118 K inhibitory activity was dependent upon its focal contact localization.

119 targeting sequence from FAK resulted in the focal contacts localization of the chimeric molecule and

120 Labeled focal contacts migrate at about 0.1 mm/min in stationary

121 lpha 5 beta 1 are able to adhere to FN, form focal contacts, migrate on FN, and assemble FN matrix.

122 but dramatically inhibited stress fiber and focal contact motility and turnover.

123 nctionally for the loss of alpha 5 beta 1 in focal contacts of alpha 5-null cells.

124 vity were present at cell-cell junctions and focal contacts of proliferating cells.

125 o substratum and distribution of vinculin in focal contacts of synemin-silenced astrocytoma cells wer

126 The alphavbeta1-3-1 mutant is recruited to focal contacts on fibrinogen and vitronectin, suggesting

127 M-7 is not concentrated in paxillin-positive focal contacts or stable focal adhesions.

128 ion to substratum, cell growth, formation of focal contacts, or formation of stress fibers.

129 t have been observed at the plasma membrane, focal contacts, or mitochondria under certain conditions

130 atable mutant, did not undergo spreading and focal contact organization on fibronectin, whereas cells

131 may be its contribution to the formation of focal contacts, particularly those involving the fibrone

132 is mediated primarily by osteoblast adhesion/focal contact pattern, viability, proliferation and diff

133 kinase 1 (PAK1) and oxidatively modified the focal contact phosphatase PTP-PEST.

134 udy that sublethal injury results in loss of focal contacts present in uninjured MPT cells, and that

135 In WT PTP phi-overexpressing cells, the focal contact protein paxillin is selectively depleted f

136 pithelial markers CK-7, CK-8, and CK-19, the focal contact protein paxillin, and the mesenchymal mark

137 ent stress fiber formation and Rho-dependent focal contact protein phosphorylation were also inhibite

138 and p125(FAK) to tyrosine phosphorylation of focal contact proteins.

139 is bleached across a beta3 integrin-labeled focal contact, recovery is complete within 16 min.

140 e redistribution of focal adhesion kinase to focal contact regions of the cytoplasm membrane, and thi

141 Actin filament remodeling, focal contact remodeling, and molecular motors are coord

142 protein tyrosine phosphatase 1B to sites of focal contact resulting in potential interactions with s

143 F-actin polymerization and the formation of focal contact rings in neutrophils, which are prerequisi

144 TRAF4 directly associated with the focal contact scaffold Hic-5, and the knockdown of eithe

145 esion kinase (FAK) acts as an adaptor at the focal contacts serving as a junction between the extrace

146 the FAK-CT domain (Pyk2/FAK-CT) localized to focal contact sites and enhanced fibronectin (FN)-stimul

147 uch as vinculin, talin, and alpha-actinin at focal contact sites in the alpha3-deficient keratinocyte

148 Localization of integrin receptors to focal contact sites occurs upon ligand binding.

149 s when localized to beta-integrin-containing focal contact sites via interactions mediated by the FAK

150 duced Rho-dependent integrin clustering into focal contact sites, which was essential for cell adhesi

151 dimers, the latter of which were situated at focal contact sites.

152 d phosphotyrosine are known to colocalize at focal contacts, sites of adhesion of cells to the extrac

153 ading defects involving a notable absence of focal contact structures and the formation of multiple s

154 e reappearance of organized actin fibers and focal contacts, suggesting MAPK as the effector pathway.

155 nert transmembrane anchor, we found that the focal contact targeting region within focal adhesion kin

156 In contrast, recovery of bleached focal contacts that contain GFP-beta3 integrin takes lon

157 Recovery of signal in bleached focal contacts that have incorporated actinin-1 is rapid

158 ctin receptor alpha(v)beta(3) remains within focal contacts, the fibronectin receptor alpha(5)beta(1)

159 on to fibronectin or laminin and coupling of focal contacts to actin-containing cytoskeleton were pre

160 vation and mediate VASP re-localization from focal contacts to the leading edge region.

161 , cellular morphology, the cytoskeleton, and focal contacts undergo significant changes.

162 he cytoskeletal protein paxillin localize to focal contacts upon adhesion to vitronectin.

163 s revealed that a fraction of SHP-2 moves to focal contacts upon integrin engagement and that SHP-2 b

164 axillinDeltaLD4 mutants, PKL localization to focal contacts was disrupted, whereas that of focal adhe

165 tion of integrins, paxillin, and vinculin at focal contacts was impaired.

166 r inducing organization of stress fibers and focal contacts was located in a 29-amino acid segment of

167 gain insight into the dynamic properties of focal contacts, we induced expression of green fluoresce

168 Small focal contacts were also observed with tubulovesicular s

169 tly, organization of the actin filaments and focal contacts were markedly changed in Wdpcp-deficient

170 ts in increased cytoskeletal interactions at focal contacts within extracellular matrices involving i